Local anesthesia is the most widely used method of pain control in dental practice. It involves injecting local anesthetic drugs near nerves to reversibly block nerve conduction and sensation in a specific part of the body. The first local anesthetic used was cocaine, extracted in 1859. Modern local anesthetics like lidocaine and bupivacaine reversibly block sodium channels, preventing nerve impulse propagation. They are metabolized in the liver and may cause minor complications like pain on injection or transient numbness, but rarely major issues. Proper dosage and technique help ensure safe and effective local anesthesia for dental procedures.

1. LOCAL ANESTHESIA
-By Dr Ekta Dwivedi

2. Contents-
 Introduction
 History
 Definition
 Indications
 Contraindications
 Ideal properties
 Classification
 Composition
 Mechanism of action
 Biotransformation
 Dosage
 Complications
 Conclusion
 References

3. Introduction
 Most widely used method of pain control in
dental practice
 Even with major advances in sedative and
General anesthesia techniques ,local
anesthetics remain the pharmacological
mainstay of a typical oral surgery practice

4. History
 Horace Wells (1844) ,first used nitrous oxide for
anesthesia in tooth extraction.
 First local anesthetic to be described was cocaine.
 Albert Niemann (1859),German chemist-first to extract
and isolate cocaine.
 On 15th September of 1884 ,Koller used cocaine for
treating glaucoma.
 William Halsted,American surgeon,developed principles
of nerve block.
 In November 1884,he performed infraorbital and inferior
alveolar nerve block.
 1901 –Epinephrine ,first used as vasoconstrictor along with
local anesthetics.

5. Definition
 Local anesthesia
 Local anesthetics

6. Advantages
 Patient remains awake and co-operative
 Low incidence of morbidity
 Patient leaves the office unescorted
 No additional trained personnel required
 Techniques not difficult to master
 Percentage of failure is small
 No additional expense to patients
 Patient need not omit the previous meal
 Little distortion of normal physiology,used to
advantage on poor risk patients

7. Indications:
 Extraction of teeth
 Odontectomy or surgical removal of teeth
 Alveoloplasty & Alveolectomy
 Incision and drainage
 Cavity preparation - in deeper painful cavities
 Pulpotomy and Pulpectomy
 Periodontal and Gingival surgeries
 Cyst enucleation and Marsupialization
 Removal of residual infection , small neoplastic growths , salivary
stones
 For relief from sore spots of dentures
 Treatment of trismus
 Therapy in trigeminal neuralgia
 In radiotherapy when patient is gagging due to placement of film
 For anesthesia of oral cavity and jaw bones in treatment of fracture

8. Contraindications
 Fear and apprehension
 Infection rules out the use of regional anesthesia
 Allergic to local anesthetics
 Below the age of reason
 Patient with mental deficiencies
 Major oral surgery makes it unfeasible
 Anamolies makes it difficult or impossible
 Patients with cardiac problems, Liver disorders,
Renal disorders
 Specific local anesthetics in famial disorders

9. Ideal Properties
 Non irritating
 Not cause permanent alteration of nerve structure
 Low systemic toxicity
 Effective when injected or locally applied
 Time of onset should be short
 Sufficient duration of action
 Potency sufficient to give complete anesthesia
 Free from producing allergic reactions
 Should be stable in solution and undergo
biotransformation readily
 Sterile or capable of being sterlized by heat
without deterioration
 Action must be reversible

10. Classification
1. According to the biological site
a . Agents acting at the receptor site on the external
surface of nerve membrane
Tetrodotoxin,saxitoxin
b. Acting on receptor site on the internal surface of
nerve membrane
quarternary ammonium analogues of Lidocaine,
scorpion venom
c. Agents acting by a receptor independent physio-
chemical mechanism
Benzocaine
d. Agents acting by combination of receptor and
receptor independent mechanism
Lidocaine, mepivacaine, prilocaine

11. 2. According to the duration of action
a. Ultra short-acting (<30 mins)
Procaine without vasoconstrictor
2% chloroprocaine without vasoconstrictor
b. Short acting(45-75 mins)
2% lidocaine with 1:100000 epinephrine
2% mepivacaine with 1:20000 levonordefrine
c. Medium acting(90-150 mins)
4% prilocaine with 1:200000 epinephrine
d.Long acting(180 mins or longer)
5% Bupivacaine with 1:200000 epinephrine

12. 3. According to chemical groups
Ester groups –
Benzoic acid ester - cocaine
benzocaine
Para aminobenzoic acid ester
procaine , tetracaine
propoxycaine
Non –ester group –
a. Anilides – bupivacaine
etidocaine
lidocaine
mepivacaine
prilocaine

13. 4. According to sources
a. Natural : cocaine
b. Synthetic nitrogenous :
Derivatives of PABA: Procaine, Benzocaine
Derivatives of acetanilide:Lidocaine
Quinoline derivatives:Cinchocaine
Acridine derivatives: Bucricaine
c.Synthetic non-nitrogenous :
Benzyl alcohol ,
d. Miscellaneous drugs with local action:
Clove oil, phenol, chlorpromazine,
antihistaminics like Diphenhydramine

14. 5. According to potency and duration of
action
a. Low potency & short duration
Procaine, chloroprocaine
b. Intermediate potency & duration
Lidocaine, Mepivacaine
c. High potency & long duration
Tetracaine, Bupivacaine

15. Composition
1. Local anesthetic agent -21.3 mgml
2. Vasoconstrictors - 0.005 mgml
3. Reducing agents like
Sodium metabisulphite -0.5 mgml
4. Preservatives like Methyl paraben
-1 gmml
5. Fungicide - Thymol
6. Vehicle - Ringers lactate -6mgml

16. Mode and site of action :
Theories of Regional Anesthesia:
1. Acetyl choline theory
2. Calcium displacement theory
3. Surface charge theory
4 .Membrane expansion theory
5. Specific receptor theory

17. Membrane expansion theory

18. Specific receptor theory

19. Electrophysiology of nerve
conduction

20. Mechanism of action
Following sequence is proposed for the
mechanism of action
1. Displacement of calcium ions from nerve receptor
site
2. Binding of local anesthetic molecule to this
receptor site
3. Bockade of the sodium channel
4. Decrease in sodium conductance
5. Depression of rate of electrical depolarization
6. Failure to achieve the threshold potential level
7. Lack of development of propogated action
potential
8. Conduction blockade

21. Mechanism of action in normal pH
 L.A available as solutions of acid salts of weak bases
 L.A weak base(BNHOH) combined with strong acid(HCL) to
make acid salt(BNHCL) solouble for use in solution
 Acid salt(BNHCL) must dissociate into free base
 Charged amino group(BNH+) dissociates outside nerve sheath
resulting in non-ionised Lipophilic molecule(BN)
 Diffuses readily through the lipid composed nerve sheath
 Combines with hydrogen ion(H+) produced from the Buffer
system
 Results in the formationof an ionised hydrophyllic L.A
molecule(BNH+)
 Displaces calcium gate
 Provides a more impermeable gate for the influx of sodium
ions

22. In infected or inflamed areas
 Inflammatory process produces acidic
products
 pH is 5 to 6 (normal tissue pH-7.4)
 Prevents deprotonization (conversion of
RNH+ to RN ) and liberation of free base
 Results in poor anesthesia

23. Biotransformation
 Ester type local anesthetics are hydrolysed in plasma by
pseudocholinesterase. Procaine, tetracaine, chloroprocaine
 Some hydrolysis also occurs in liver
 Atypical pseudocholinesterase –heriditary trait-relative
contraindication
 Excreted in small concentrations in urine
 Amide type of L.A- primary site of biotransformation is
Liver (70% of dose injected)
 Relative contraindication in patients with Liver, Hepatic,
and cardiac failures
 Present in urine as the parent compound in greater %


24. Nerve block

25. Field block

26. Local infiltration

27. Intraligamentary technique

28. Submucosal analgesia

29. Paraperiosteal analgesia

30. Intraosseous analgesia

31. Anesthetic complications
 Definition
 Classification
1. Primary Secondary
2. Mild Severe
3. Transient Permanent
4. Those attributed to the solution used
toxicity , idiosyncracy , allergy , infections
5.Those attributed to the insertion of needle
syncope , trismus , pain , edema

32. COMPLICATIONS
Local complications
Systemic complications

33. Local complications
1. Needle breakage
2. Pain on injection
3. Burning on injection
4. Persistent anesthesia or Paresthesia
5. Trismus
6. Hematoma
7. Infection
8. Edema
9. Sloughing of tissues
10. Lip chewing
11. Facial nerve paralysis
12Post anesthetic intraoral lesions

34. Systemic complications
1.Syncope
2.Toxicity Overdosage
Predisposing factors
Patient factors Drug factors
-age - vasoactivity
- weight - concentration
- other drugs - dose
- sex - route of admn
- diseases - rate of injection
- genetics - vascularity of inj site
- mental attitude - vasoconstrictors

35.  Toxic effects on C .N. S-
Cortical stimulation
Cortical depression
Medullary stimulation
Medullary depression
Toxic effects on C. V .S -

36. Toxic effects on respiratory system
Allergic reactions:
Symptoms
Treatment
Prevention

37. Elevated blood levels of L.A may result
from:
1.Large dose administration
2. Rapid absorbtion from the site of injection
3. Intravascular administration of L.A
4.Unusually slow Biotransformation of the
drug
5.Decreased rate of elimination of the drug

38. Dosage

39. References
 Monheim”s :Local anesthesia & pain
control in Dental practice
 Stanley.F.Malamed:Hand book of L.A
 Allan Donald : Dental Analgesia &
anesthesia
 Tripathi:Pharmacology